Reflections of using low dose tren <300mg a week(long read)

[Rido]

To those who run sub-250… like 70-120mg per week.

Do you pin daily? Or eod? I know the most beneficial would be daily; for the efficacy. Just curious what you guys have done in the past?

I fucking hate pinning daily. Shit turns into a nightmare after about 6 weeks.

I’ve been too much of a puss to try the slin pin sub injections.

Thanks all

There are 3 different esters. The dose is pretty low and I think anyone should be able to handle the sides of that range.

 

[DollaBill]

Shit. I totally forgot to write ace.

My bad. My brain sometimes skips steps when I get excited talking about shit.

But yeah, Tren Ace.

I have the same fucking problem. The only sides that are big issues for me are the negative mindset, the hatred, easily pissed off… and I get those sides almost right away. It’s shitty. And my girls the one who gets most of those sides.. so I fucking hate myself for taking it. But, seeing low dosage might help out with the sides.. well that’s optimistic, especially because I have a ton of it

 

[GuerillaPete]

Shit. I totally forgot to write ace.

My bad. My brain sometimes skips steps when I get excited talking about shit.

But yeah, Tren Ace.

I have the same fucking problem. The only sides that are big issues for me are the negative mindset, the hatred, easily pissed off… and I get those sides almost right away. It’s shitty. And my girls the one who gets most of those sides.. so I fucking hate myself for taking it. But, seeing low dosage might help out with the sides.. well that’s optimistic, especially because I have a ton of it

I did eod with ace.
Short ester i can compare Ed and EoD is propionate i did both and felt no different.

 

[DollaBill]

I have always done Eod with higher doses. I just wanted to hear everyone else’s experience with low doses. Especially if it helps with the negative mindset

 

[Mac11wildcat]

I am a hard supporter of every day pins for short esters. It’s calmed down like 90% of expected sides from all drugs, namely tren. Shouldn’t be on ace for more than 4-6 weeks anyways.

 

[DollaBill]

Maybe I should buy some 25g pins instead of my normal 23’s.. suck it up and do em every day

 

[Deadp007]

Maybe I should buy some 25g pins instead of my normal 23’s.. suck it up and do em every day

How many mL's would you be injecting daily?
Use insulin pins, you should be able to get shallow IM...
@Mac11wildcat what do you use for daily inj's?

 

[Mac11wildcat]

How many mL's would you be injecting daily?
Use insulin pins, you should be able to get shallow IM...
@Mac11wildcat what do you use for daily inj's?

Just about everything I pin goes thru a 25g loading pin and then however many 1cc 29g 1/2” needles as is needed. I stay lean enough for slins basically year round, and so far it’s been far better for me (I get some pretty bad PIP on usually benign compounds and regularly just get “bad” pins but using slins daily has reduced it immensely).

 

[DollaBill]

god damn. I need to work harder and get as lean as you. 29g sounds absolutely beautiful compared to my 23’s

 

[effswithtren]

I am a hard supporter of every day pins for short esters. It’s calmed down like 90% of expected sides from all drugs, namely tren. Shouldn’t be on ace for more than 4-6 weeks anyways.

When I was young and dumb I did some dumb shot with Tren A. Besides the dumb dosages I had no business playing with, I started out EOD because I hated pinning. It was a fucking nightmare of sides. Swapping to ED fixed almost all of them (at least, as much as one could expect from 700mg of fucking tren A).

 

[AbstractMind]

Sure, so Recomp is really a goal or outcome of a dietary & training (& drug) regimen, like fat loss or bulking. Whereas fat loss is defined as decreased FM & retention of LBM, Recomp is defined as increased LBM & decreased FM (fat mass).

Partitioning is a concept that serves the goal of all rational dietary interventions. The p-ratio (partitioning ratio) describes protein deposited in LBM tissues relative to energy intake and, conversely, protein lost from LBM tissues relative to energy deficit. The p-ratio encompasses the factors of i) hormone status (i.e., absolute levels of known key hormones), ii) insulin sensitivity, & iii) leptin sensitivity. There is an interplay between i) - iii).

Insulin sensitivity: when dieting (i.e., in a state of energy deficit), Insulin resistance enhances fat loss by limiting the muscle's use of glucose for fuel - sparing glucose
for use by the brain & ↑intramuscular FA utilization . When bulking, insulin sensitivity within muscle is good & in fat cells bad:

For example: individuals with poor skeletal muscle insulin sensitivity overproduce insulin; store more kcal in AT (why they have more trouble getting "the pump").

Factors that affect insulin sensitivity include: i) b.f.% (primary predictor): ↑b.f. ⇒ ↑FA substrates for fuel (sparing glucose & protein) & dictates adipokine signaling (i.e., adipocyte-secreting hormones [Leptin, TNF-α, IL-..., adiponectin, etc.]), ii) diet: HI CHO (especially refined), saturated fat & low fiber ⇒ ↓insulin sensitivity, iii) muscular contraction ⇒ ↑insulin sensitivity (by ↑glucose uptake into muscle cell; GLUT4 translocation), iv) glycogen depletion ⇒ ↑insulin sensitivity (why though?)... this contradicts later passages where glycogen depletion is said to promote insulin resistance, by sparing glucose & promoting FA oxidation by increasing the use of FA substrates as energy to perform work... the resulting increased blood FA concentrations further promote insulin resistance, v) genetic factors (... another day)
Leptin is an adipokine hormone, secreted primarily by adipocytes, correlate with b.f.%, ↑b.f. ⇒ ↑Leptin. (Visceral vs. subcutaneous depots have different relationships to Leptin). At any given b.f.%, women produce ~2-3x Leptin vs. men. Δ with energy restriction & overfeeding. Leptin is a primary energy storage regulatory signal that reflects: i) b.f. % & ii) energy intake

Example 1: Upon initiating a diet, Leptin may decline by 50% within 1 week (or less) - although obviously have not lost 50% b.f. - so acutely, Leptin Δ become unrelated to b.f. (rather signaling energy intake)

After the initial decline, there is a more gradual decline in leptin related to b.f. loss.

Example 2: Upon overfeeding, leptin similarly ↑rapidly (a without a relationship to Δb.f. )

In the short term, leptin secretion primarily determined by glucose availability - such that pulling glucose out of the fat cell (dieting) ⇒ ↓Leptin & vice versa

Leptin hormone's site-specific effects include effects on the pancreas & liver, in skeletal muscle it ↑FA & ↓AA & glucose use as fuel substrates (enhancing fat loss, promoting protein sparing)....

I could go on for days about this.

Essentially, partitioning is a concept that couples leptin & insulin sensitvity (as these are principal factors in how changes in caloric intake (and macronutrient content) affect metabolism (influencing body composition profoundly) as well as hormonal status. We can tweak and enhance it.

P-ratio factors into all aspects of dietary interventions and we want to enhance p-ratio whether recomping, bulking, or cutting.

Can you shed some light on your statement that insulin resistance is good for fat loss? From my understanding, high amounts of blood sugar typically lead to weight and ultimately fat gain. Always enjoy your posts.

 

[Jaxino]

I used tren in high doses for 3-4y and now after 7y on gear i can say that none really needs more that 300-400 TrenE/A a week. OK if you are Nick Walker going to win the Mr.O, 700mg will be a walk in the park, but look at how much muscle this guy carries on.

Atm i am taking my bb journey much easier:
-A lot of good food
-750 TestE/Sust
600 EQ
300 TrenE
6iu HGH
Humalog (4-6iu) AM Prewo Postwo OR of Humalin R with prewo meal.

When i used more Tren or much more gear in general it hindered my gains, i was sleeping like shit, digestion was so so, basically couldn't eat enough/rest to grow.

Tren is a very strong molecule and there's no need to go crazy with it.
Sorry GH15.....

 

[Smashshit]

god damn. I need to work harder and get as lean as you. 29g sounds absolutely beautiful compared to my 23’s

I use 27-29g slin pins always and I’m not very lean and have no issues.

 

[Type-IIx]

Can you shed some light on your statement that insulin resistance is good for fat loss? From my understanding, high amounts of blood sugar typically lead to weight and ultimately fat gain. Always enjoy your posts.

I'll do what I can in a post, but please recognize that to learn and appreciate fully insulin resistance as a concept could take up most a full course of study in its own right, so this is going to be my best attempt.

First, do not confuse the enhancement of insulin resistance on fat loss with any judgment of insulin resistance being a state that I advocate for, or think is healthy in sedentary individuals; this is obviously unhealthy, associated with the metabolic syndrome, diabetes, not to mind central abdominal adiposity, etc.

Insulin resistance is a state wherein the body's tissues (e.g., liver, pancreas, skeletal muscle) no longer recognizes the body's insulin and continues to produce glucose in inappropriately high quantities (the effect rather than causative, though toxic levels of glucose do degrade the pancreatic islet cells' responsiveness to insulin as one pathway/mechanism of insulin resistance, feeding back to worsen insulin resistance).

As we know, fat loss occurs with the GLP-1 & GIP agonists that are insulin sensitizing. Still, it is not insulin sensitivity per se that is responsible for this effect - indeed high blood glucose in itself neither enhances fat gain nor inhibits fat loss - but rather, fat loss occurs due to the other effects of these drugs such as altered food preferences, delayed gastric emptying, satiation, that promote appetite control and reduce energy intake.

In fact, the vast majority of fat loss agents promote insulin resistance, e.g., β-agonists, stimulant drugs like caffeine and ephedrine, these all either act analogously to or increase the action of catecholamines (epinephrine, norepinephrine, or adrenaline and noradrelanine).

When tissues like the liver and fat cells fail to be stimulated by insulin, glucose is not taken up by the cells. Without glucose, the liver begins to metabolize free-fatty acids (increasing ketone levels in the blood), preventing them from being re-esterified into fat cells. In liver & fat cells, without insulin being taken up into these tissues, there is suppression of fat synthesis/lipogenesis (adipocyte) & VLDL synthesis (liver).

Let's not forget the brain; when systemic blood glucose is elevated, it'll constantly have its favored energy source and keep us alive. We like that.

This might all sound perfectly rosy, but we like how the GLP-1 & GIP agonists work because insulin resistance during caloric restriction in skeletal muscle (70ish% of our cells, more in bodybuilders) is sort of a scary image, glycogen stores are first catabolized; then intramuscular triglyceride, and eventually, if the body has to, it will use proteins for energy to perform work.

 

[AbstractMind]

I'll do what I can in a post, but please recognize that to learn and appreciate fully insulin resistance as a concept could take up most a full course of study in its own right, so this is going to be my best attempt.

First, do not confuse the enhancement of insulin resistance on fat loss with any judgment of insulin resistance being a state that I advocate for, or think is healthy in sedentary individuals; this is obviously unhealthy, associated with the metabolic syndrome, diabetes, not to mind central abdominal adiposity, etc.

Insulin resistance is a state wherein the body's tissues (e.g., liver, pancreas, skeletal muscle) no longer recognizes the body's insulin and continues to produce glucose in inappropriately high quantities (the effect rather than causative, though toxic levels of glucose do degrade the pancreatic islet cells' responsiveness to insulin as one pathway/mechanism of insulin resistance, feeding back to worsen insulin resistance).

As we know, fat loss occurs with the GLP-1 & GIP agonists that are insulin sensitizing. Still, it is not insulin sensitivity per se that is responsible for this effect - indeed high blood glucose in itself neither enhances fat gain nor inhibits fat loss - but rather, fat loss occurs due to the other effects of these drugs such as altered food preferences, delayed gastric emptying, satiation, that promote appetite control and reduce energy intake.

In fact, the vast majority of fat loss agents promote insulin resistance, e.g., β-agonists, stimulant drugs like caffeine and ephedrine, these all either act analogously to or increase the action of catecholamines (epinephrine, norepinephrine, or adrenaline and noradrelanine).

When tissues like the liver and fat cells fail to be stimulated by insulin, glucose is not taken up by the cells. Without glucose, the liver begins to metabolize free-fatty acids (increasing ketone levels in the blood), preventing them from being re-esterified into fat cells. In liver & fat cells, without insulin being taken up into these tissues, there is suppression of fat synthesis/lipogenesis (adipocyte) & VLDL synthesis (liver).

Let's not forget the brain; when systemic blood glucose is elevated, it'll constantly have its favored energy source and keep us alive. We like that.

This might all sound perfectly rosy, but we like how the GLP-1 & GIP agonists work because insulin resistance during caloric restriction in skeletal muscle (70ish% of our cells, more in bodybuilders) is sort of a scary image, glycogen stores are first catabolized; then intramuscular triglyceride, and eventually, if the body has to, it will use proteins for energy to perform work.

I’ve never thought of that, how the insulin response in different tissue types can vary and have different effects. That’s super cool and extremely complex man.

 

[grey]

My experience has been similar with Tren... these days when I use it I run even lower (my limit for sides seems to be roughly ~200mg/week) with much larger amounts of Masteron and only my TRT dose of Test.

Anything higher than that level of Tren and I experience pretty much all of your sides along with truly fucked up night sweat levels.

 

[Adg99]

My experience has been similar with Tren... these days when I use it I run even lower (my limit for sides seems to be roughly ~200mg/week) with much larger amounts of Masteron and only my TRT dose of Test.

Anything higher than that level of Tren and I experience pretty much all of your sides along with truly fucked up night sweat levels.

How high above test can you go with mast before you feel crashed e2 symptoms? I’m scared too push it.

 

[grey]

How high above test can you go with mast before you feel crashed e2 symptoms? I’m scared too push it.

Never had an issue with it personally so I can't say.

I generally use 800 mg/week of Masteron if I use it at all.

Have gone as high as 1600mg/wk before realizing that it really wasn't doing anything additional for me at that level but still didn't have any issues.

 

[Rido]

Never had an issue with it personally so I can't say.

I generally use 800 mg/week of Masteron if I use it at all.

Have gone as high as 1600mg/wk before realizing that it really wasn't doing anything additional for me at that level but still didn't have any issues.

I was wondering who else runs mast this high. Any hair problems? I don't have mpb and haven't had issues on 600

 

[grey]

I was wondering who else runs mast this high. Any hair problems? I don't have mpb and haven't had issues on 600

No issues but I also don't have the gene for it.
If it ends happening I will just try to rock the Kojak.